A University of California at San Francisco-led team presented CRISPR-based strategies to systematically repress and activate the transcription of endogenous human genes. As they report online in Cell, the researchers started by screening the activity of short guide RNAs (sgRNAs) tiling to sequences in and around transcription start sites for dozens of genes mediating ricin susceptibility in cells. From there, they detected patterns associated with activation or repression, ultimately developing genome-scale libraries of CRISPR repressors, called CRISPRi, and CRISPR activators (CRISPRa) that they used for subsequent screens for genes related to cell growth features.
Researchers from the Massachusetts Institute of Technology and the Broad Institute's Stanley Center for Psychiatric Research describe the development of modified mice that can be used to perform CRISPR-Cas9 experiments both in vivo and ex vivo using either viral or non-viral sgRNA delivery methods. In proof-of-principle experiments, for instance, the team demonstrated that they could use this system to study cancer in the mice, creating conditions that diminished the function of tumor suppressor genes or enhanced the activity of apparent oncogenes.
Using germ-free mice, 16S ribosomal RNA sequencing, and shotgun pyrosequencing, a team from the US and France tracked the microbial community members that take up residence in the mouse gut over time following exposure to different bacterial sources — from soil to gut bugs from other organisms such as humans, zebrafish, or termites. For instance, their findings delineated the types of microbial community succession that takes place during different types of exposures, including ongoing dominance by microbial species introduced from soil sources. In addition, the study's authors argued the strategy they used "generalizes to address a variety of mechanistic questions about succession, including succession in the context of microbiota-directed therapeutics."